Our previous studies have shown that there may be a functional relationship between benzodiazepine (BZ) receptor stimulation and alterations in calcium flux. Nifedipine, a calcium channel blocker, prevented the sleep-inducing effects of flurazepam in rats. Conversely, as we reported last year, a calcium channel agonist (Bay K 8644) potentiates the effects of flurazepam. This year we have examined the specificity of the effects of nifedipine with respect to other actions of BZ. Nifedipine did not block the effects of diazepam in increasing punished drinking in a model for anxiolytic effects of drugs. Nifedipine also did not block anticonvulsant effects of diazepam. Calcium channels may play a more important role in sleep induction than in other actions of BZ. We also showed that sleep-inducing effects of pentobarbital were not susceptible to blockade by nifedipine, indicating that the role of calcium channels in sleep may be specific for BZ; that is, barbiturates may cause sleep through a mechanism that does not require changes in Ca2+ flux.